Di (2-ethylhexyl) phthalate reduces sperm motility by decreasing sperm tail energy supply

Abstract

Di (2-ethylhexyl) phthalate (DEHP) is widespread in the environment. It can impair sperm function through damaging the sperm development process. However, few studies have focused on the sperm tail that is directly related to sperm motility. In this study, we demonstrate that DEHP impedes the conversion of riboflavin in the mitochondrial sheath in the midsection of the sperm tail, resulting in reduced ATP (adenosine triphosphate) synthesis, thereby inhibiting sperm motility. The results of HPLC-MS/MS showed that DEHP metabolites were transported to the testes and epididium, indicating that MEHP (Mono-2-ethylexyl phthalate) could directly affect the espermatozoa of mature. Sperm motility analysis determined that sperm motility decreased with increasing DEHP concentration. The movement of sperm is mainly dependent on the tail motility, which is largely determined by tail structure and energy supply. Electron microscopy images illustrate that there are no observable changes in the basic kinematic structure of the sperm tail. However, DEHP causes a decrease in complex II activity of mitochondrial respiratory chain by interfering with the synthesis of the cofactor FAD (Flavin adenine dinucleotide), which leads to a decrease in ATP concentration. Therefore, DEHP exposure can reduce sperm motility by decreasing sperm tail energy supply. This study exemplifies the importance of the sperm tail in sperm dysfunction caused by environmental pollutants.

Keywords

• Di (2-ethylhexyl) phthalate (DEHP)
• Motility of sperm
• Sperm tail
• FAD
• Riboflavin